Allergy and Hypersensitivity Flashcards
With examples, give the different types of hypersensitivity reactions.
- TYPE 1 - IgE mediated. EXAMPLE - ANAPHYLAXIS
- TYPE II - Antibody dependant eg IgG or IgM. EXAMPLE - Haemolytic anaemia
- TYPE III - Immune complex mediated. EXAMPLE - SLE
- TYPE IV - T-Cell mediated. EXAMPLE - Rash
Describe what occurs in Type 1 hypersensitivity reactions. PART 1
- CD4+ T helper cells activate B cells - produce IgE antibodies specific to antigen
- Antibodies bind to Fc receptors on surface of mast cells and basophils
- Cells become sensitised. Immediate response on re-exposure to same allergen.
Describe what occurs in Type 1 hypersensitivity reactions. PART 2
- Allergen cross links bound IgE on sensitised cells - causes anaphylactic degranulation.
- Chemical mediators e.g histamines and cytokines released
- Vasodilation and smooth muscle contraction occurs
What mast cell mediators cause vasodilation and increased permeability, and smooth uscle spasms?
- Histamines/PAF/ Prostaglandin D2/ Leukotriene C4/D4/E4
What causes leuocycte extravasation?
- Cytokines
- Chemotactic factors for neutrophils and eosinophils
Describe bronchial asthma
- Chronic inflammation with intermittent/reversible airway obstruction
- Dominated by presence of eosinophils, CD4+ cells and CD4+ NK cells expressing invariant TCR - recognises antigens
What causes the following and what are the responses?
- WHEAL AND FLARE
- ALLERGIC RHINITIS
- FOOD ALLERGY
- WHEAL AND FLARE - Insect bites. Route of entry is subcutaenous and causes local increase in blood flow.
- ALLERGIC RHINITIS - Caused by pollens when inhaled causing inflammation of nasal mucosa.
- FOOD ALLERGY - Orally. Causes vomiting but progresses to anaphylaxis
What are some treatments for Type 1 hypersensitivity reactions?
- IMMUNOTHERAPY - Allergy shots/ ANTIHISTIAMINES AND ANTI-INFLAMMATORIES
Describe anaphylaxis.
- Severe reaction to allergens causing body wide degranulation of mast cells. Causes vasodilation and shock
- Evoked by direct exposure or being in presence of allergen
What are some risk factors of anaphylaxis?
- Age-related factors
- Co-existing diseases
- Concurrent medications
- Emotional stress and acute infections
How can anaphylaxis be identified?
- Sudden reductions in BP
- Sudden skin, GI and respiratory symptoms
- Itching, generalised hives and swollen tongue, lips etc.
How can anaphylaxis be treated? PART 1
- Remove exposure to trigger
- Assess airway, breathing and circulation
- Call for help
- Inject epinephrine intramuscularly into mid-anterolateral aspect of thigh
- Place patient on back or position of comfort if respiratory distress and/or vomiting
How can anaphylaxis be treated? PART 2
- Elevate lower extremities - can be fatal if patient sits/stands suddenly
- When indicated, give high-flow supplemental oxygen by face mask
- Establish IV access using needles and give 1-2 litres of saline rapidly
- Perform CPR and continuously check patient vitals
Describe Type II hypersensitivity reactions.
- IgG and IgM antibodies directed against antigens on host cells
- Leads to cell lysis or tissue damage through complement (in)dependent mechanisms
- Results in opsonisation, cell lysis by MAC and RBC agglutination
Describe complement dependent Type II hypersensitivity reactions.
- Antibody targets antigens on host cells
- Ab-Ag complexes activate complement causing cell lysis by MAC or opsonisation with C4 causing other immune cells to phagocytose opsonised material
- Caused by incompatible blood transfusions, autoimmune haemolytic anaemia and Goodpasture’s syndrome
Describe antibody dependent cell mediated cytotoxicity in Type II hypersensitivity reactions.
- Low concentrations of IgG coat target cells
- Inflammatory cells e.g NK cells and granulocytes bind to IgG via Fc receptors and lyse target cells using perforins.
- Occurs during transplant rejection, immune reactions against neoplasms/parasites
Describe HDN.
- Occurs when immune system develop antibodies against baby’s RBCs causing haemolysis
- If mother is Rh- and carries Rh+ fetus, anti-Rh antibodies produced i.e IgG antibodies (anti-D antibodies)
- Cross placenta into fetal circulation and lead to haemolysis
- Treated with antibodies to the Rh antigen - no anti-D antibody production
Describe Type III hypersensitivity reactions.
- Generation of Ab-Ag immune complexes inducing inflammation
- Antigens bind to antibodies and form immune complexes which deposit in tissues
- Activates complement clasical pathway and recruits neutrophils and macrophages causing inflammation
- Causes inflammation and tissue injury
Describe serum sickness.
- Occurs when patients administered serum from healthy people (containing antibodies beneficial to patients)
- Antibodies produced against antigens in donor’s serum
- Deposition of Ab-Ag complexes in kidneys and joints
- Can cause glomerulonephritis and arthritis
Describe the characteristics of Type IV hypersensitivity.
- T-cell mediated NOT ANTIBODY MEDIATED
- Reaction takes several days to develop
What is the mechanism of Type IV hypersensitivity reactions?
- CD4+ T helper cells recognise antigens in complex with MHC Class II on surface of APCs
- CD4+ T cells secrete IL-2 inducing further cytokine release
- Activated CD8+ T cells destroy target cells and activated macrophages produce hydrolytic enzymes.
- Overreaction of cells and overproduction of cytokines causes inflammation and cell death.
Describe the tuberculin skin test. PART 1
- Determines if patient infected with Mycobacterium tuberculosis
- Antigen injected subcutaenously and processed by APCs
- Th1 cell recognises antigen and releases cytokines - act on vascular endothelium
Describe the tuberculin skin test. PART 2
- Recruitment of phagocytes and plasma to site of injection
- Produces pale elevation of skin
